Tumor-driving gene may be able to prevent nerve pain caused by chemotherapy
RICHMOND, Va. (WRIC) -- There may be a strategy that regulates inflammation responsible for causing nerve pain due to chemotherapy-induced side effects of treatment, according to research from Virginia Commonwealth University (VCU).
According to a Wednesday release from VCU, the center suggested that a tumor-driving gene -- AEG-1 -- can prevent nerve pain responsible for causing chemotherapy-induced peripheral neuropathy (CIPN).
Previous research said that chemotherapy drugs can cause inflammation throughout the body, which can affect a patient's nerve endings. This is one of the main contributors to the pain with CIPN.
“Currently, there are no FDA-approved medications designed to specifically treat or prevent CIPN in cancer patients, and the current clinical approach for the management of it is inadequate,” said study author M. Imad Damaj, Ph.D., member of the Cancer Prevention and Control research program at Massey and a professor in the Department of Pharmacology and Toxicology at the VCU School of Medicine. “Our findings could help pave the way for the development of an entirely new and effective therapeutic option for CIPN.”
VCU said that common symptoms include pain, tingling, numbness or sensitivity in the hands or feet caused by damage to the nervous system. This reportedly can help patients manage their treatment dose and if there is too much pain, can stop the chemotherapy regimen altogether.
Some patients with CIPN are prescribed opioids, which, according to VCU, an addictive pain medications -- platinum-based drugs and taxanes.
“One of the major advantages supported by our findings is that we’ve identified a promising strategy through which we can pursue new targeted treatments as an alternative to more addictive pain medications,” said study co-author Devanand Sarkar, MBBS, Ph.D., the associate director for research training and education who holds the Harrison Foundation Distinguished Professorship in Cancer Research at Massey, as well as a professor of cellular, molecular and genetic medicine at the VCU School of Medicine.
The research team deleted the gene within the cells, which can inhibit the inflammation in the brain and "overall preventing the onset of CIPN," according to VCU.
The research team said that more research needs to be conducted to evaluate the effectiveness of the targeted treatments to prevent CIPN -- this would be through clinical trials. However, researchers will need to determine if there is a way a treatment strategy can reverse any effects of CIPN in patients.
“If effective, this double weapon approach may represent a holistic therapeutic strategy that can be utilized to prevent both cancer progression and chemotoxicity, which could drastically improve survivorship and quality of life for patients diagnosed with cancer,” Damaj said.